Haemodynamic Effects of Different Beta Blockers in Angina Pectoris

1977 ◽  
Vol 22 (1) ◽  
pp. 64-68 ◽  
Author(s):  
H. Åström ◽  
B. Jonsson

Beta-blocking agents with partial agonist activity seem to reduce heart rate at rest slightly less than those without this property. Cardio-selective drugs have no effect on stroke volume at rest contrary to the non-selective ones which will reduce it somewhat. This difference is abolished during exercise. The only difference seen during work between different beta-blockers is the effect on the peripheral vascular resistance. The selective drugs lower the arterial pressure with unchanged resistance.

1964 ◽  
Vol 19 (3) ◽  
pp. 457-464 ◽  
Author(s):  
Burton S. Tabakin ◽  
John S. Hanson ◽  
Thornton W. Merriam ◽  
Edgar J. Caldwell

The physiologic variables defining the circulatory and respiratory state in normal man have been measured in recumbency, standing at rest and during progressively severe grades of exercise approaching near-maximal levels. Indicator-dilution technique was used for determination of cardiac output with simultaneous radio-electrocardiographic recordings of heart rate. Direct intra-arterial pressure measurements were utilized for calculation of peripheral vascular resistance. Minute volume of ventilation, oxygen utilization, and carbon dioxide elimination were obtained from analysis of expired air collected at the time of each cardiac output determination. A peak mean workload of 1,501 kg-m/min was realized during the treadmill exercise. Increases in cardiac output over the range of exercise employed correlated well with indices of workload such as heart rate, oxygen utilization, and minute volume of ventilation. There was no correlation of stroke volume with these indices. It is concluded from examination of individual stroke-volume responses that a progressive increase in stroke volume is not a necessary or constant phenomenon in adapting to increasing workload. cardiac output in treadmill exercise; dye-dilution cardiac output determinations; arterial pressure during upright exercise; stroke-volume response to graded treadmill exercise; exercise response of cardiac output and stroke volume; peripheral vascular resistance response to position and exercise; treadmill exercise—effects on cardiac output, stroke volume, and oxygen uptake; minute ventilation, cardiac output, and stroke volume during exercise; carbon dioxide elimination during treadmill exercise; heart rate and cardiac output during treadmill exercise; exercise; physiology Submitted on July 12, 1963


2007 ◽  
Vol 112 (3) ◽  
pp. 193-201 ◽  
Author(s):  
Jan T. Groothuis ◽  
Nynke van Dijk ◽  
Walter ter Woerds ◽  
Wouter Wieling ◽  
Maria T. E. Hopman

In patients with orthostatic intolerance, the mechanisms to maintain BP (blood pressure) fail. A physical counter-manoeuvre to postpone or even prevent orthostatic intolerance in these patients is leg crossing combined with muscle tensing. Although the central haemodynamic effects of physical counter-manoeuvres are well documented, not much is known about the peripheral haemodynamic events. Therefore the purpose of the present study was to examine the peripheral haemodynamic effects of leg crossing combined with muscle tensing during 70° head-up tilt. Healthy subjects (n=13) were monitored for 10 min in the supine position followed by 10 min in 70° head-up tilt and, finally, for 2 min of leg crossing with muscle tensing in 70° head-up tilt. MAP (mean arterial BP), heart rate, stroke volume, cardiac output and total peripheral resistance were measured continuously by Portapres. Leg blood flow was measured using Doppler ultrasound. Leg vascular conductance was calculated as leg blood flow/MAP. A significant increase in MAP (13 mmHg), stroke volume (27%) and cardiac output (18%), a significant decrease in heart rate (−5 beats/min) and no change in total peripheral resistance during the physical counter-manoeuvre were observed when compared with baseline 70° head-up tilt. A significant increase in leg blood flow (325 ml/min) and leg vascular conductance (2.9 arbitrary units) were seen during the physical counter-manoeuvre when compared with baseline 70° head-up tilt. In conclusion, the present study indicates that the physical counter-manoeuvre of leg crossing combined with muscle tensing clearly enhances leg blood flow and, at the same time, elevates MAP.


1989 ◽  
Vol 17 (4) ◽  
pp. 466-469 ◽  
Author(s):  
J. Tibballs ◽  
S. Sutherland ◽  
S. Kerr

The haemodynanic effects of Brown Snake (Pseudonaja) species (textilis, nuchalis, affinis) were investigated in anaesthetised, mechanically ventilated dogs. Blood pressure decreased to minimal levels five minutes after intravenous envenomation. Hypotension was accompanied by significant decrements in cardiac output and stroke volume and a rise in peripheral vascular resistance. Heart rate increased transiently during 0.5-2.0 minutes after envenomation but had declined below resting levels five minutes after envenomation. No statistically significant change was recorded in central venous pressure. Depression of myocardial contractility is postulated as the mechanism of venom induced hypotension.


Cephalalgia ◽  
1982 ◽  
Vol 2 (1) ◽  
pp. 33-45 ◽  
Author(s):  
K. Weerasuriya ◽  
L. Patel ◽  
P. Turner

Except for propranolol, no other b-blocker has been studied thoroughly in the prophylaxis of migraine. Of those studied, propranolol, atenolol and timolol were shown to be useful in double-blind clinical trials. The mode, or even the site of action of these drugs is unknown. Possible mechanisms of action are peripheral vascular effects, a central action, 5-HT antagonism, an anxiolytic effect and a multifactorial action. The only common property of the successful drugs is lack of partial agonist activity and their profiles do not fully support any of the above hypotheses. Trials of drugs in the prophylaxis of migraine have in general been unsatisfactory due to the difficulty in controlling many variables. b-blockers with differing properties offer an opportunity to define the properties necessary for anti-migraine activity and perhaps shed light on the pathogenesis of migraine.


1988 ◽  
Vol 52 (1) ◽  
pp. 60-65
Author(s):  
TOYOZO HASHIMOTO ◽  
KAZUOKI KONDO ◽  
TERUHIKO TOYO-OKA ◽  
KEN-ICHI KAWASAKI ◽  
SAICHI HOSODA ◽  
...  

1970 ◽  
Vol 48 (7) ◽  
pp. 481-489 ◽  
Author(s):  
D. Regoli

Propranolol (10 to 30 μg/kg), oxprenolol (trasicor) (5 to 10 μg/kg), and sotalol (10 to 50 μg/kg) evoke an acute and prolonged increase of arterial pressure in normal and nephrectomized rats, while after adrenalectomy the arterial pressure remains unchanged or is reduced. The pressor effect is accompanied by a reduction of heart rate. The dose of the three beta blockers evoking an arterial pressure increase does not antagonize the effect of isopropylnoradrenaline. To block the beta receptors, doses 10 to 100 times higher than those effective on arterial pressure have to be used. The block of the beta receptors is accompanied by an initial fall of the blood pressure and by a significant decrease of the heart rate. The pressor effect of beta blockers is not antagonized but rather is potentiated by phenoxybenzamine and phentolamine. Moreover, in the presence of an alpha receptor blockade, the administration of beta blockers partially restores the response to catecholamines. These results support the hypothesis that the pressor effect evoked by beta receptor blocking agents may be due: (a) to the release of endogenous catecholamines and (b) to the interference by beta blockers with phenoxybenzamine and phentolamine on the alpha receptors.


1974 ◽  
Vol 48 (s2) ◽  
pp. 65s-67s ◽  
Author(s):  
C. F. George ◽  
P. J. Lewis ◽  
J. A. Steiner ◽  
C. T. Dollery

1. The effects of propranolol and R03-4787, a new beta-adrenoceptor antagonist with a partial agonist activity, have been studied in a blind, cross-over comparison with placebo. 2. In ten patients who completed the study, the two drugs produced a similar reduction in blood pressure; the reduction in heart rate with propranolol was significantly(P0.001)greater than that produced by R03-4787. 3. Plasma renin activity averaged 4.13 ± 1.37 ng h−1ml−1 on placebo, fell to 3.64 ± 1.47 ng h−1ml−1 on propranolol and to 2.50 ± 1.39 ngh−1ml−1 on R03-4787. 4. No correlation was demonstrable between the log plasma concentration of either propranolol or R03-4787 and change in blood pressure.


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